scholarly journals Bradykinin and changes in microvascular permeability in the hamster cheek pouch: role of nitric oxide

1996 ◽  
Vol 118 (6) ◽  
pp. 1371-1376 ◽  
Author(s):  
M. Félétou ◽  
E. Bonnardel ◽  
E. Canet
Keyword(s):  
Nitric Oxide ◽  
Microvascular Permeability ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch

Nitric oxide accounts for histamine-induced increases in macromolecular extravasation

1994 ◽  
Vol 266 (6) ◽  
pp. H2369-H2373 ◽  
Author(s):  
W. G. Mayhan
Keyword(s):  
Nitric Oxide ◽  
Fluorescent Microscopy ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Before And After ◽  
Subsequent Activation ◽  
Ly 83583

The goal of this study was to determine the role of nitric oxide in histamine-induced increases in macromolecular extravasation in the hamster cheek pouch in vivo. We used intravital fluorescent microscopy and fluorescein isothiocyanate dextran (FITC-dextran; mol wt = 70,000 K) to examine extravasation from postcapillary venules in response to histamine before and after application of an enzymatic inhibitor of nitric oxide, NG-monomethyl-L-arginine (L-NMMA; 1.0 microM). Increases in extravasation of macromolecules were quantitated counting the number of venular leaky sites. Histamine (1.0 and 5.0 microM) increased the number of venular leaky sites from zero (basal conditions) to 11 +/- 1 and 21 +/- 2/0.11 cm2, respectively. Superfusion of L-NMMA (1.0 microM) and LY-83583 (1.0 microM) significantly decreased histamine-induced formation of venular leaky sites, whereas L-arginine (100 microM) potentiated histamine-induced formation of venular leaky sites. In contrast, superfusion of NG-monomethyl-D-arginine (1.0 microM) did not inhibit the formation of venular leaky sites in response to histamine. Thus the findings of the present study suggest that production of nitric oxide, and subsequent activation of guanylate cyclase, plays an important role in macromolecular efflux in vivo in response to histamine.

Nicotine impairs histamine-induced increases in macromolecular efflux: role of oxygen radicals

1998 ◽  
Vol 84 (5) ◽  
pp. 1589-1595 ◽  
Author(s):  
William G. Mayhan ◽  
Glenda M. Sharpe
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Smokeless Tobacco ◽  
Oxygen Radicals ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Macromolecular Transport ◽  
Before And After ◽  
Oxide Synthase

Nicotine, a major component of cigarettes and smokeless tobacco, has toxic effects on endothelium and impairs reactivity of resistance arterioles in response to agonists that stimulate the synthesis and/or release of nitric oxide. However, the effect of nicotine on nitric oxide synthase-dependent increases in macromolecular transport is not known. Thus our first goal was to determine the effect of nicotine on histamine-induced increases in macromolecular efflux. We used intravital microscopy and FITC dextran (mol wt 70,000) (FITC-dextran-70K) to examine macromolecular extravasation from postcapillary venules in response to histamine before and after intravenous infusion of vehicle or nicotine. Extravasation of macromolecules was quantitated by counting venular leaky sites and calculating clearance (ml/s × 10−6) of FITC-dextran-70K. Histamine elicited reproducible increases in venular leaky sites and clearance in hamsters infused with vehicle. In contrast, nicotine infusion inhibited histamine-induced increases in macromolecular efflux. Histamine (1.0 and 5.0 μM) elicited 19 ± 2 and 34 ± 4 vs. 3 ± 1 and 11 ± 5 leaky sites per 0.11 cm2, before vs. after nicotine infusion, respectively ( P < 0.05). Histamine-induced clearance of FITC-dextran-70K was also impaired after infusion of nicotine. Our second goal was to examine whether alterations in histamine-induced increases in macromolecular efflux by nicotine may be related to the production of oxygen radicals. Application of superoxide dismutase (150 U/ml) to the hamster cheek pouch restored histamine-induced increases in venular leaky sites and clearance of FITC-dextran-70K during infusion of nicotine. Thus nicotine alters agonist-induced increases in microvascular permeability, via the formation of oxygen radicals, to presumably inactivate nitric oxide.

Role of nitric oxide in capillary perfusion and oxygen delivery regulation during systemic hypoxia

2005 ◽  
Vol 288 (2) ◽  
pp. H525-H531 ◽  
Author(s):  
Silvia Bertuglia ◽  
Andrea Giusti
Keyword(s):  
Nitric Oxide ◽  
Lipid Peroxide ◽  
Cheek Pouch ◽  
Capillary Perfusion ◽  
Hamster Cheek Pouch ◽  
No Donor ◽  
Phosphorescence Quenching ◽  
Systemic Hypoxia ◽  
Synthase Inhibitor

The role of nitric oxide (NO) and reactive oxygen species (ROS) in regulating capillary perfusion was studied in the hamster cheek pouch model during normoxia and after 20 min of exposure to 10% O2-90% N2. We measured Po2 by using phosphorescence quenching microscopy and ROS production in systemic blood. Identical experiments were performed after treatment with the NO synthase inhibitor NG-monomethyl-l-arginine (l-NMMA) and after the reinfusion of the NO donor 2,2′-(hydroxynitrosohydrazono)bis-etanamine (DETA/NO) after treatment with l-NMMA. Hypoxia caused a significant decrease in the systemic Po2. During normoxia, arteriolar intravascular Po2 decreased progressively from 47.0 ± 3.5 mmHg in the larger arterioles to 28.0 ± 2.5 mmHg in the terminal arterioles; conversely, intravascular Po2 was 7–14 mmHg and approximately uniform in all arterioles. Tissue Po2 was 85% of baseline. Hypoxia significantly dilated arterioles, reduced blood flow, and increased capillary perfusion (15%) and ROS (72%) relative to baseline. Administration of l-NMMA during hypoxia further reduced capillary perfusion to 47% of baseline and increased ROS to 34% of baseline, both changes being significant. Tissue Po2 was reduced by 33% versus the hypoxic group. Administration of DETA/NO after l-NMMA caused vasodilation, normalized ROS, and increased capillary perfusion and tissue Po2. These results indicate that during normoxia, oxygen is supplied to the tissue mostly by the arterioles, whereas in hypoxia, oxygen is supplied to tissue by capillaries by a NO concentration-dependent mechanism that controls capillary perfusion and tissue Po2, involving capillary endothelial cell responses to the decrease in lipid peroxide formation controlled by NO availability during low Po2 conditions.

Role of nitric oxide in leukotriene C4-induced increases in microvascular transport

1993 ◽  
Vol 265 (1) ◽  
pp. H409-H414 ◽  
Author(s):  
W. G. Mayhan
Keyword(s):  
Nitric Oxide ◽  
Fluorescent Microscopy ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Leukotriene C4 ◽  
Hamster Cheek Pouch ◽  
Macromolecular Transport ◽  
Transport Of Macromolecules

The goal of this study was to determine the role of nitric oxide in alterations in macromolecular transport of the hamster cheek pouch in vivo in response to leukotriene C4. We used intravital fluorescent microscopy to examine the transport of macromolecules across the hamster cheek pouch in response to leukotriene C4 before and after application of an enzymatic inhibitor of nitric oxide, NG-monomethyl-L-arginine (L-NMMA; 1.0 microM). Increases in transport of macromolecules across the hamster cheek pouch were quantitated by the formation of venular leaky sites and clearance of fluorescein isothiocyanate-dextran (FITC-dextran; mol wt = 70 K). Leukotriene C4 (1.0 and 3.0 nM) produced an increase in the number of venular leaky sites and clearance of FITC-dextran-70K. Superfusion of L-NMMA (1.0 microM) significantly decreased leukotriene C4-induced increases in venular leaky sites and clearance of FITC-dextran-70K. In addition, superfusion of LY-83583 (10 microM) significantly decreased leukotriene C4-induced increases in venular leaky sites. In contrast, superfusion of NG-monomethyl-D-arginine (D-NMMA; 1.0 microM), indomethacin (10 mg/kg iv), or diphenhydramine hydrochloride; 15–20 mg/kg iv) did not significantly alter leukotriene C4-induced increases in venular leaky sites. Thus these findings suggest that production of nitric oxide and subsequent activation of guanylate cyclase play an important role in formation of venular leaky sites and clearance of FITC-dextran-70K in response to application of leukotriene C4.

In vivo assessment of microvascular nitric oxide production and its relation with blood flow

2001 ◽  
Vol 280 (3) ◽  
pp. H1222-H1231 ◽  
Author(s):  
X. F. Figueroa ◽  
A. D. Martínez ◽  
D. R. González ◽  
P. I. Jara ◽  
S. Ayala ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Plasma Flow ◽  
Subcellular Fractionation ◽  
No Synthase ◽  
Cheek Pouch ◽  
No Production ◽  
Hamster Cheek Pouch ◽  
Membrane Bound

To assess the hypothesis that microvascular nitric oxide (NO) is critical to maintain blood flow and solute exchange, we quantified NO production in the hamster cheek pouch in vivo, correlating it with vascular dynamics. Hamsters (100–120 g) were anesthetized and prepared for measurement of microvessel diameters by intravital microscopy, of plasma flow by isotopic sodium clearance, and of NO production by chemiluminescence. Analysis of endothelial NO synthase (eNOS) location by immunocytochemistry and subcellular fractionation revealed that eNOS was present in arterioles and venules and was 67 ± 7% membrane bound. Basal NO release was 60.1 ± 5.1 pM/min ( n = 35), and plasma flow was 2.95 ± 0.27 μl/min ( n = 29). Local NO synthase inhibition with 30 μM N ω-nitro-l-arginine reduced NO production to 8.6 ± 2.6 pmol/min (−83 ± 5%, n = 9) and plasma flow to 1.95 ± 0.15 μl/min (−28 ± 12%, n = 17) within 30–45 min, in parallel with constriction of arterioles (9–14%) and venules (19–25%). The effects of N ω-nitro-l-arginine (10–30 μM) were proportional to basal microvascular conductance ( r = 0.7, P < 0.05) and fully prevented by 1 mM l-arginine. We conclude that in this tissue, NO production contributes to 35–50% of resting microvascular conductance and plasma-tissue exchange.

Role of EDHF in conduction of vasodilation along hamster cheek pouch arterioles in vivo

2000 ◽  
Vol 278 (6) ◽  
pp. H1832-H1839 ◽  
Author(s):  
Donald G. Welsh ◽  
Steven S. Segal
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Cytochrome P 450 ◽  
Arteriolar Diameter

We tested whether local and conducted responses to ACh depend on factors released from endothelial cells (EC) in cheek pouch arterioles of anesthetized hamsters. ACh was delivered from a micropipette (1 s, 500 nA), while arteriolar diameter (rest, ∼40 μm) was monitored at the site of application (local) and at 520 and 1,040 μm upstream (conducted). Under control conditions, ACh elicited local (22–65 μm) and conducted (14–44 μm) vasodilation. Indomethacin (10 μM) had no effect, whereas N ω-nitro-l-arginine (100 μM) reduced local and conducted vasodilation by 5–8% ( P < 0.05). Miconazole (10 μM) or 17-octadecynoic acid (17-ODYA; 10 μM) diminished local vasodilation by 15–20% and conducted responses by 50–70% ( P < 0.05), suggesting a role for cytochrome P-450 (CYP) metabolites in arteriolar responses to ACh. Membrane potential ( E m) was recorded in smooth muscle cells (SMC) and in EC identified with dye labeling. At rest (control E m, typically −30 mV), ACh evoked local (15–32 mV) and conducted (6–31 mV) hyperpolarizations in SMC and EC. Miconazole inhibited SMC and EC hyperpolarization, whereas 17-ODYA inhibited hyperpolarization of SMC but not of EC. Findings indicate that ACh-induced release of CYP metabolites from arteriolar EC evoke SMC hyperpolarization that contributes substantively to conducted vasodilation.

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